Pancreas Flashcards

1
Q

Physical examination in pancreatic disease

A
  • Position against pain- ‘lean on all four’
  • Cullen,
  • Grey-Turner signs- in severe acute cases
  • skin nodules- occasionally, due to fat necrosis (extensor skin surfaces)
  • Rarely- retinopathy- temp/perm.blindness in severe acute cases igns of malnutrition- in chronic cases fever
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2
Q

Acute pancreatitis etiology

A

I= idiopathic
G= gallstone
E=ethanol
T= trauma
S= steroids
M= mumps (infections)
A=autoimmune dis.
S= scorpion sting (toxins) H= hypercalcemia, hypertriglycerides
E= endoscopic colangiography
D= drugs

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3
Q

Manifestation in acute pancreatitis

A
  • – Pain: upper abd-epigastric, severe, steady, radiating to back
  • The duration of pain varies but typically lasts >24hs
  • Nausea, vomiting, diarrhoea, loss of appetite –
  • Systemic manif: sev form
  • -dyspnea- pleural eff., acute respiratory distress sdr.
  • Tenderness at the palpation of epigatsrium; guarding; often ileus
  • Severe cases: hemodynamic instability
  • Grey-Turner, Cullen: hemorrhagic form
  • Rare- jaundice Muscle spasms- sec.to hypocalcemia
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4
Q

Acute pancreatitis colementary examination

A

– Enzymes: elevated levels of amylase, lipase, at least 3 times above the reference range  erum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 1-2 weeks after treatment.  Amylase: increases also in salivary gland diseases, Imaging tests macroamylasemia  The levels don’t correlate with the severity

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5
Q

Forms of acute pancreatitis

A

– Mild- localized manifestations

– Severe- necrosis- followed by
systemic inflam.response

  • Resp.changes: pleural effusion, dyspnea- irritation of the diaphragm, acute respiratory distress syndrome
  • hemodynamic instability
  • Cullen, Grey signs
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6
Q

Ransom criteria

A

Criteria present on admission : -patient older than 55 years -WBC count higher than 16,000/µL -Blood glucose level higher than 200 mg/dL -Serum L H level higher than 350 IU/L -A T level higher than 250 IU/L Criteria developing during the first 48 hours : -Hematocrit fall more than 10% -BUN level increased by more than 8 mg/dL -Serum calcium level lower than 8 mg/dL -Pa o2 less than 60 mm Hg -Base deficit higher than 4 mEq/L -Estimated fluid sequestration higher than 600 mL

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7
Q

Ranson score

A

Each of the above criteria counts for 1 point. A Ranson score of 0-2 has a minimal mortality A Ranson score of 3-5 has a 10-20% mortality rate, and the patient should be admitted to the intensive care unit A Ranson score higher than 5 after 48 hours has a mortality of more than 50% and is associated with more systemic complications.

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8
Q

Complication acute pancreatitis

A
  • By definition, peripancreatic fluid collections persisting for more than 4 weeks are termed acute pseudocysts Infected pancreatic necrosis
  • Abscess
  • pancreatic duct disruption
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9
Q

Etiology of chronic pancreatitis

A
  • Alcohol abuse
  • ! Obstruction: congenital abnormalities (pancreas divisum) and acquired forms (trauma – trauma and ductal strictures) Hypercalcemia Hyperlipidemia
  • Tropical pancreatitis
  • autoimmune
  • Inherited disorders: pancreatic secretory serine protease inhibitor mutation gene (ad); cystic fibrosis
  • Idiopathic: 30% of cases
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10
Q

Clinical manifestation in chronic pancreatitis

A
  • Pain: chronic pain/ intermittent ’attack” - pain severity either decreases or resolves over 5-25 years
  • . steatorrhea (caused by fat malabsorption, resulting in bulky, foul-smelling stools that may appear oily and float)
  • *Weight loss**
  • diabetes- 10 years >90% of the pancreas is destroyed maldigestion (due to decreased intraluminal hydrolysis of food)
  • Signs of manutrition
  • During attack”: flexion of the knees
  • Possible mass in the epigastrium - palpation
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11
Q

Diabetics mellitus type 1

A

Type 1= circulating insulin is very low or absent, plasma glucagon is elevated, and the pancreatic beta cells fail to respond to all insulin-secretory stimuli. – Autoimmunity – Usually up to age of 40 – strong genetic component

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12
Q

Diabetes type 2

A

Type 2 = peripheral insulin resistance with an insulin-secretory defect

– Maturity-onset diabetes of the young (M Y) is a form of type 2 diabetes that affects many generations in the same family with an onset in individuals younger than 25 years.

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13
Q

Risk factor of diabetes mellitus type2

A
  • Age - older than 45 years
  • Obesity
  • Family history of type 2 diabetes in a first-degree relative
  • Hispanic, Native American, African American, Asian American, or acific Islander descent History of previous impaired glucose tolerance (IGT) or impaired fasting glucose (I G)
  • Hypertension (>140/90 mm Hg) or dyslipidemia
  • History of delivering a baby with a birth weight of >4kg
  • Polycystic ovarian syndrome (which results in insulin resistance)
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14
Q

Who diabetes criteria

A

Diabetes

  • Fasting plasma glucose ≥7.0mmol/l (126mg/dl) or 2-h
  • plasma glucose ≥11.1mmol/l (200mg/dl)

Impaired Glucose tolerance (IGt)

  • Fasting plasma glucose n<7.0mmol/l (126mg/dl)
  • 2–h plasma glucose ≥7.8 and <11.1mmol/l (between 140mg/dl and 200mg/dl)

Impaired fasting Glucose (IfG)

  • Fasting plasma glucose 6.1 to 6.9mmol/l (110mg/dl to 125mg/dl)
  • 2–h plasma glucose and (if measured) <7.8mmol/l (140mg/dl)
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15
Q

manifestation of diabetes

A

-PPPGBFMN

  • Polyuria and thirst: olyuria is due to osmotic diuresis secondary to hyperglycemia. Thirst is due to the hyperosmolar state and dehydration.
    • Polyphagia with weight loss: The weight loss with a normal or increased appetite is due to depletion of water and a catabolic state
  • Gastrointestinal symptoms: Nausea, abdominal discomfort or pain- in ketoacidosis
    – Chronic gastrointestinal symptoms in the later stage of diabetes are due to visceral autonomic neuropathy.
  • -Peripheral neuropathy: numbness and tingling in hands and feet, in a glove and stocking pattern. It is bilateral, symmetric, and ascending neuropathy, which results from many factors, including the accumulation of sorbitol in peripheral sensory nerves due to sustained hyperglycemia. -
  • beta cell destruction may have started months or years before the onset of clinical symptoms.
  • -fatigue and weakness: due to a catabolic state of insulin deficiency, hypovolemia, and hypokalemia. -
  • Muscle cramps: This is due to electrolyte imbalance.
  • -Nocturnal enuresis: secondary to polyuria; can be an indication of onset of diabetes in young children.
  • -Blurred vision: due to the effect of the hyperosmolar state on the lens and vitreous humor.
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16
Q

Complications of diabetes

A
  • Acute- coma: ketoacidosis (Kusmaul breathing), hypoglycemia (cold, sweat skin)
  • Chronic:
  • *Micro-: retinopathy, nephropathy, neuropathy Macro-: acceleratd atherosclerosis process  Autonomic neuropathy: pic – Increased risk for infections**
17
Q

Hypoglycemic coma

A
  • adrenergic: sweating, shakiness, tachycardia, anxiety, and a sensation of hunger
  • Neuroglycopenic: weakness, tiredness, or dizziness; inappropriate behavior, iritability, confusion; blurred vision, coma and death

symptoms of hypoglycemia are fewer in elderly and appear at a lower level of plasma glucose than in younger persons.
Type 1 DM- after insulin therapy

18
Q

Hyperglycemic coma

A
  • Hyperosmolar nonketotic coma
    – is characterized by hyperglycemia, hyperosmolarity and dehydration without significant ketoacidosis
  • ​Ketoacidotic coma
    DDDDCABP
    – In type 1 and rare in type 2 (triggered by a severe condition)
    – Polydipsia and polyuria- early symptoms
    – Dry skin and mucosa
    – Dyspneea- Kusmaul type of breathing
    – decreased skin turgor
    – decreased reflexes
    – Characteristic acetone (ketotic) breath odor
    – Abdominal pain, tenderness
    – body temperature may be within the reference range or low, even in the presence of intercurrent infection !!!!!!!!!!!!!!!!!!!
19
Q

Symptoms in pancreatic disease

A

Pain: steady, location- epigastrium, partly relieved by sitting up and leaning forwards, often with radiation to the back, and associated with vomiting.

-Pancreatic steatorrhoea- very pale, offensive, smelly and bulky stools due to malabsorption of fat; oil (triglycerides) may be passed per rectum

20
Q

pancreas compementary examination

A
  • elevations of serum amylase and lipase are found only during acute attacks of pancreatitis, usually early in the course of disease
  • low concentrations of serum trypsin are relatively specific for advanced chronic pancreatitis
  • Direct tests: the most sensitive; they can be used to detect chronic pancreatitis at its earliest stage; however, they are somewhat invasive, labor intensive, and expensive: duodenal aspiration, pancreatic juice